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From: Long-term Suppression of Neurodegeneration in Chronic Experimental Optic Neuritis: Antioxidant Gene Therapy
Invest. Ophthalmol. Vis. Sci.. 2007;48(12):5360-5370. doi:10.1167/iovs.07-0254
Figure Legend:
Microscopy of myelin and axonal loss. (A) Representative light micrograph of the control retrobulbar optic nerve from an
EAE mouse showed loss of toluidine blue staining, typical of the classical demyelination of EAE, and cellular infiltration
(arrows). Eyes treated with AAV-ECSOD (B), AAV-CAT (C), or both anti-ROS genes (D) had fewer foci of demyelination
and inflammation than the control shown in (A). (E) Transmission electron microscopy shows an inflammatory cell,
acellular spaces where axons were likely lost, and few remaining axons in the retrobulbar optic nerve of a control eye
inoculated with AAV-GFP. Some axons were naked; others were enveloped by thin sheaths of myelin (arrows) indicative
of remyelination.
The retrobulbar optic
nerve
of an eye
treated with
AAV-ECSOD
(F) had a column
of ©axons
manyreserved.
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more remaining axons than the control shown in (E). Astrocytic cells were also a prominent finding. (G) Retrobulbar optic
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